Alzheimer’s Disease Detectable In Preclinical Stage

Test Reflects Risks From Blood Transfusions

A simple blood test reliably detects signs of brain damage in people on the path to developing Alzheimer’s disease – even before they show signs of confusion and memory loss, according to a new study from Washington University School of Medicine in St. Louis and the German Center for Neurodegenerative Diseases in Germany.

The findings may one day be applied to quickly and inexpensively identify brain damage in people with not just Alzheimer’s disease but other neurodegenerative conditions such as multiple sclerosis, traumatic brain injury or stroke. The findings also indicate that deadly proteins are found in blood, which further confirms the transmissibility of neurodegenerative disease via a blood transfusion from an infected donor.

“This is something that would be easy to incorporate into a screening test in a neurology clinic,” said Brian Gordon, PhD, an assistant professor of radiology at Washington University’s Mallinckrodt Institute of Radiology and an author on the study. “We validated it in people with Alzheimer’s disease because we know their brains undergo lots of neurodegeneration, but this marker isn’t specific for Alzheimer’s disease. High levels could be a sign of many different neurological diseases and injuries.”

The test detects neurofilament light chain, a structural protein that forms part of the internal skeleton of neurons. When brain neurons are damaged or dying, the protein leaks out into the cerebrospinal fluid that bathes the brain and spinal cord and from there, into the bloodstream.

Finding high levels of the protein in a person’s
cerebrospinal fluid has been shown to provide strong evidence that some of
their brain cells have been damaged. But obtaining cerebrospinal fluid requires
a spinal tap, which many people are reluctant to undergo. Senior author Mathias
Jucker, PhD, a professor of cellular neurology at the German Center for
Neurodegenerative Diseases in Tübingen, along with Gordon and colleagues from
all over the world, studied whether levels of the protein in blood also reflect
neurological damage.

To find out whether protein blood levels could be used to
predict cognitive decline, the researchers collected data on 39 people with
disease-causing variants when they returned to the clinic an average of two
years after their last visit. The participants underwent brain scans and two
cognitive tests: the Mini-Mental State Exam and the Logical Memory test. The
researchers found that people whose blood protein levels had previously risen
rapidly were most likely to show signs of brain atrophy and diminished
cognitive abilities when they revisited the clinic.

“It will be important to confirm our findings in late-onset
Alzheimer´s disease and to define the time period over which neurofilament
changes have to be assessed for optimal clinical predictability,” said Jucker,
who leads the DIAN study in Germany.

All kinds of neurological damage can cause the neurofilament
light protein to spill out of neurons and into blood. Protein levels are high
in people with Lewy body dementia and Huntington’s disease; they rise
dramatically in people with multiple sclerosis during a flare-up and in
football players immediately after a blow to the head.

A commercial kit – very similar to the one used by the
authors – is available to test for protein levels in the blood, but it has not
been approved by the FDA to diagnose or predict an individual’s risk of brain
damage. Before such a test can be used for individual patients with Alzheimer’s
or any other neurodegenerative condition, researchers will need to determine
how much protein in the blood is too much, and how quickly protein levels can
rise before it becomes a cause for concern.

“I could see this being used in the clinic in a few years to identify signs of brain damage in individual patients,” said Gordon, who is also an assistant professor of psychological & brain sciences. “We’re not at the point we can tell people, ‘In five years you’ll have dementia.’ We are all working towards that.”

Neurodegenerative disease has been surging around the
world for the past 30 years. It’s the fastest-growing cause of death and
it will soon be the leading cause of death.

Alzheimer’s disease alone is taking the lives of 50-100
million people around the world now. The epidemic is more severe in some
countries than others. As millions die, even more will be diagnosed. Millions
more are suffering in silence with a misdiagnosis or no diagnosis. No one
really knows the scope of the epidemic. Unfortunately, one of the common
threads is the mishandling of infectious waste. A variety of factors can
trigger neurodegenerative disease, including genetics, head trauma and
neurotoxins.

Despite millions of deaths, experts suggest that the
prevalence of the disease will quadruple by 2050, if not sooner. Unfortunately,
there is a growing stack of evidence that Alzheimer’s disease, Parkinson’s
disease and other brain diseases are transmissible. They also are being
misdiagnosed and undiagnosed at an alarming rate. Deadly, self-replicating
proteins appear to be one of the common threads.

At $236 billion a year, Alzheimer’s disease is already the most expensive disease in the United States. The disease saw a 15.7 percent jump over 2014 numbers–the largest increase of all major causes of death. It accounted for 108,227 documented deaths (and thousands more of undiagnosed and undocumented ones) in the U.S. alone in 2015. A similar pattern is emerging around the globe–some regions much more than others.

In the U.S., nearly one in every five Medicare dollars is
spent on people with Alzheimer’s disease or another dementia.

Prions (PREE-ons) are a deadly and unstoppable form of
protein that migrates, mutates, multiplies and kills with unparalleled
efficiency. Prions cause fatal neurodegenerative disease in humans and
other mammals by converting the cellular version of prion protein into a toxic
form that erodes the brain and body. Prion disease often is described as a
wasting disease that causes a loss of body mass and brain mass.

Dr. Stanley Prusiner, an American neuroscientist from the
University of California at San Francisco, earned a Nobel Prize in 1997 for discovering
and characterizing prions and prion disease. President Obama awarded
Prusiner the National Medal of Science in 2010 to recognize the importance of
his research.

Prion disease also is known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” Prusiner claims that all forms of TSE are caused by infectious prions.

“There has been a resurgence of this sort of thinking, because there is now real evidence of the potential transmissibility of Alzheimer’s,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins (prions).”

A study published in the journal Nature adds to the evidence about the transmissibility of Alzheimer’s disease between people. A second study by the same scientist in early 2016 supports the claim. Meanwhile, there is absolutely no evidence to the contrary. Even wildlife and sea mammals are contracting brain disease from people because of the dumping of infectious waste on farms, ranches and forests. Yes, research has found that plants/crops grown in infectious prions uptake those prions and become infectious.

TSE is a spectrum disease that varies in severity and symptoms. It depends on which region of the brain is impacted first and by what prion mutation. Few cases are identical in terms of symptoms and diagnoses. When the presenting symptom is memory loss, the diagnoses flow along the following chart.

In humans, the prion spectrum includes Alzheimer’s disease,
Parkinson’s disease and an extremely aggressive version known as
Creutzfeldt-Jakob disease. The difference between these diseases is very slight
and often indistinguishable to neurologists. For example, millions of people
have the severe form of Alzheimer’s disease, which is known as Creutzfeldt-Jakob
disease (CJD). CJD is clearly a prion disease. According to neuroscientists Dr.
Laura Manuelidis, at least 25 percent of Alzheimer’s disease diagnoses are
actually CJD, which is further up the prion spectrum. CJD, without dispute, is
extremely infectious to caregivers and loved ones, but it has not been declared
a reportable disease across the U.S. and many other nations. Within the
continuum of care, some treat it as an infectious disease, while others don’t.

Millions of cases of deadly CJD are being misdiagnosed as
Alzheimer’s disease. Millions of patients and caregivers are being misinformed,
misguided and exposed to an aggressive prion disease. Millions of people with
prion disease have exposed us all to their infectious waste thanks to
misinformation, mismanagement and negligence.

Unfortunately, Prusiner’s science is being ignored and
we all are facing a public health disaster because of the negligence and
reckless disregard for public health.

Prion disease is highly contagious, incurable and fatal. Despite
all of the smoke and mirrors, prion disease is prion disease. It’s killing more
and more mammals, including humans, every year. The hype about species barriers
is ridiculous, reckless and irresponsible.

Victims should be quarantined because prions are in the
urine, feces, blood, saliva, mucus, skin and cell tissue of all victims–all
human byproducts that are washed, dumped, or flushed down sinks and toilets.
One can assume that the waste is extra infectious when it comes from funeral
homes, nursing homes, hospitals, dental offices, veterinarians, slaughterhouses
and some laboratories.

Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process can’t stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. Wastewater treatment plants are spreading infectious waste far and wide because they are incapable of stopping prions. As such, all by-products and discharges from wastewater treatment plants are infectious waste, which are contributing to the global epidemic of neurodegenerative disease among humans, wildlife and livestock.

The U.S. Environmental Protection Agency (EPA) has
confirmed that prions are in sewage and that there has been no way to detect
them or stop them. As such, the EPA has never issued guidance on prion
management within wastewater treatment plants. Unfortunately, the EPA’s risk
assessment on sewage sludge and biosolids were prepared
before the world of science knew about prions. The agency continues to cling to
its antiquated sludge rule crafted back in the dark ages. It does, however,
consider prions a “emerging contaminant of concern.” Meanwhile, its outdated
risk assessments are promoting a public health disaster. The neurotoxins found
in sewage, including heavy metals, also are contributing to the global spike
in autism, which follows the
same timing and trajectory as the spike in neurodegenerative diseases.

“Since it’s unlikely that the sewage treatment process can
effectively deactivate prions, adopting measures to prevent the entry of prions
into the sewer system is advisable,” said the Toronto Department of
Health, November 2004.

Once unleashed on the environment, prions remain infectious.
They migrate, mutate and multiply as they infect crops, water supplies,
wildlife, livestock, sea mammals and humans. According to prion researcher Joel
Pedersen at the University of Wisconsin, prions in soil become up to 680 times
more infectious. From there, they migrate, mutate and multiply. It’s a real
world version of Pandora’s Lunchbox.

“Our results suggest that if prions enter municipal
wastewater treatment systems, most of the agent would bond to sewage sludge,
survive anaerobic digestion, and be present in treated biosolids,” Pedersen
said. “Land application of biosolids containing prions represents a route for
their unintentional introduction into the environment. Our results
emphasize the importance of keeping prions out of municipal wastewater
treatment systems.”

Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.

The risk assessments prepared by the U.S. EPA for wastewater
treatment and sewage sludge are flawed and current practices of
recycling this infectious waste is fueling a public health disaster. Many risks
are not addressed, including prions and radioactive waste. They don’t mention
prions or radiation because there is no answer. Most nations are making the
same mistake. We’re dumping killer proteins on crops, parks, golf courses,
gardens, ski areas, school grounds and beyond. Wind, rain and irrigation spread
these contaminants and many more throughout our communities and watersheds.

Failure to account for known risks is negligent. Crops for humans and livestock grown in sewage sludge absorb prions and become infectious. We’re all vulnerable to neurotoxins and right now due to widespread denial and mismanagement. It’s time to stop the land application of sewage sludge (LASS) in all nations. Safer alternatives exist.

Preview and order the eBook now
to defend yourself and your family. There is no prevention and no cure, but
smart nutrition can save your life. If you have brain disease, nutrition is
your best hope for treatment.

Gary
Chandler is a prion expert. He is
the CEO of Crossbow Communications, author of several books and producer of documentaries
about health and environmental issues around the world. Chandler is connecting
the dots to the global surge in neurodegenerative disease, including Alzheimer’s
disease, Parkinson’s
disease, Creutzfeldt-Jakob
disease, chronic
wasting disease and other forms of prion disease. The scientific name for
prion disease is transmissible spongiform encephalopathy. The operative word is
“transmissible.” Even the global surge in autism appears to be related.

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